Statement of the Problem: It has been known that the concentration of serum prolactin (PRL) in lung cancer patients is higher than in healthy people. Recent reports point out that the PRL expression level of lung cancer tissues is related to patients’ survival rate. The lower survival rate occurs in patients who have higher PRL expression level. The aim of this study was to investigate the stimulatory mechanism of PRL in non-small cell lung cancer cells. Methodology & Theoretical Orientation: We detected the effect of PRL on cell proliferation by MTT assay. The results show that cell proliferation was significantly increased after treatment with PRL by 50 nM for 24 h. We also detected cell proliferation related signaling pathway JAK2/STAT3 and EMT (Epithelial–mesenchymal transition) marker by western blot. Findings: The protein levels of p-JAK2 and p-STAT3 were significantly increased after treatment with PRL. We also analyzed STAT3- regulated downstream gene VEGF mRNA level and protein level by qRT-PCR and western blot. VEGF mRNA and protein levels were significantly increased by PRL. The protein expressions of p-JAK2, p-STAT3 and VEGF were inhibited by JAK2 inhibitor AZD1480. AZD1480 treatment also led reduction of cell proliferation. Not only cell proliferation but also metastasis were led low survival rate in lung cancer patients. Results show that PRL also enhanced the protein levels of N-cadherin and vimentin. The protein expression of E-cadherin was decreased after treatment with PRL. Conclusion & Significance: These results suggested that PRL might promote NSCLC cells cell proliferation which was regulated through JAK2/STAT3 signaling pathway and EMT. The mechanism of stimulatory effects on PRL might be a target on NSCLC therapy in the future.
